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CYP2D6

Cytochrome P450 2D6 (CYP2D6) is an enzyme that in

humans is encoded by the CYP2D6 gene. CYP2D6 is primarily
expressed in the liver. It is also highly expressed in areas of
the central nervous system, including the substantia nigra.

CYP2D6, a member of the cytochrome P450 mixed-function

oxidase system, is one of the most important enzymes
involved in the metabolism of xenobiotics in the body. In
particular, CYP2D6 is responsible for the metabolism and
elimination of approximately 25% of clinically used drugs, via
the addition or removal of certain functional groups –
specifically, hydroxylation, demethylation, and dealkylation.[3]
CYP2D6 also activates some prodrugs. This enzyme also
metabolizes several endogenous substances, such as
hydroxytryptamines, neurosteroids, and both m-tyramine and
p-tyramine which CYP2D6 metabolizes
CYP2D6
into dopamine in the brain and liver.[3][4]

Considerable variation exists in the

efficiency and amount of CYP2D6
enzyme produced between individuals.
Available
Hence, for drugs that are metabolized
structures
by CYP2D6 (that is, are CYP2D6
PDB Human
substrates), certain individuals will
UniProt
eliminate these drugs quickly
search: PDBe
(ultrarapid metabolizers) while others
RCSB
slowly (poor metabolizers). If a drug is
List of PDB
metabolized too quickly, it may
id codes
decrease the drug's efficacy while if the
drug is metabolized too slowly, toxicity 2F9Q,
may result.[5] So, the dose of the drug 3QM4,

may have to be adjusted to take into 3TBG,

3TDA,
account of the speed at which it is
4WNT,
metabolized by CYP2D6.[6]
4WNU,

Other drugs may function as inhibitors 4WNV,

4WNW,
of CYP2D6 activity or inducers of
4XRY, 4XRZ
CYP2D6 enzyme expression that will
lead to decreased or increased CYP2D6
activity respectively. If such a drug is Identifiers
taken at the same time as a second Aliases CYP2D6,
CPD6,
drug that is a CYP2D6 substrate, the
CYP2D,
first drug may affect the elimination
CYP2D7AP,
rate of the second through what is
CYP2D7BP,
known as a drug-drug interaction.[5] CYP2D7P2,
CYP2D8P2,
Gene CYP2DL1,
CYPIID6,
The gene is located near two
P450-DB1,
cytochrome P450 pseudogenes on P450C2D,
chromosome 22q13.1. Alternatively P450DB1,
spliced transcript variants encoding cytochrome
different isoforms have been found for P450 family
this gene.[7] 2 subfamily
D member
6,
Genotype/phenotype
Cytochrome
variability P450 2D6

CYP2D6 shows the largest

phenotypical variability among the External OMIM:
IDs 124030
CYPs, largely due to genetic
HomoloGen
polymorphism. The genotype accounts
133550
for normal, reduced, and non-existent
CYP2D6 function in subjects. GeneCards:
Pharmacogenomic tests are now CYP2D6
Gene location (H
available to identify patients with
variations in the CYP2D6 allele and
have been shown to have widespread
Chr. Chromosome
use in clinical practice.[8] The CYP2D6
(human)[1]
function in any particular subject may
be described as one of the following:[9]
Band 22q13.2 Start
poor metabolizer – little or no
CYP2D6 function End
intermediate metabolizers –
metabolize drugs at a rate
RNA expression
somewhere between the poor and pattern
extensive metabolizers
extensive metabolizer – normal
CYP2D6 function
ultrarapid metabolizer – multiple
copies of the CYP2D6 gene are
expressed, so greater-than-normal
CYP2D6 function occurs

A patient's CYP2D6 phenotype is often More reference

clinically determined via the expression data
administration of debrisoquine (a Gene ontolog
selective CYP2D6 substrate) and
Molecular • iron ion
subsequent plasma concentration
function binding
assay of the debrisoquine metabolite • metal i
(4-hydroxydebrisoquine).[10] binding
• heme b
The type of CYP2D6 function of an
•
individual may influence the person's oxidored
response to different doses of drugs activity,
that CYP2D6 metabolizes. The nature on paire
of the effect on the drug response donors,
depends not only on the type of incorpor
reductio
CYP2D6 function, but also on the
molecul
extent to which processing of the drug
oxygen
by CYP2D6 results in a chemical that
• drug bi
has an effect that is similar, stronger, or
•
weaker than the original drug, or no oxidored
effect at all. For example, if CYP2D6 activity
converts a drug that has a strong effect • aromat
into a substance that has a weaker activity

effect, then poor metabolizers (weak •

oxidored
CYP2D6 function) will have an
activity,
exaggerated response to the drug and
on paire
stronger side-effects; conversely, if donors,
CYP2D6 converts a different drug into a incorpor

substance that has a greater effect reductio

molecul
than its parent chemical, then ultrarapid
oxygen,
metabolizers (strong CYP2D6 function)
flavin or
will have an exaggerated response to
flavopro
the drug and stronger side-effects.[11] one don
incorpor
Genetic basis of variability one atom
oxygen
The genetic basis for CYP2D6-
• steroid
mediated metabolic variability is the hydroxyl
CYP2D6 allele, located on chromosome activity
22. Subjects possessing certain allelic •
variants will show normal, decreased, monoox
or no CYP2D6 function, depending on activity

the allele. Pharmacogenomic tests are Cellular • organe

now available to identify patients with component membra

variations in the CYP2D6 allele and • endopl

reticulum
have been shown to have widespread
membra
use in clinical practice.[8]
• membr
• intrace
membra
CYP2D6 enzyme activity for bounded

selected alles[12][13] organell

• endopl
CYP2D6
Allele reticulum
activity
• mitoch
CYP2D6*1 normal • cytopla
CYP2D6*2 normal
Biological • steroid
CYP2D6*3 none process metabol
CYP2D6*4 none process
CYP2D6*5 none • alkaloid
metabol
CYP2D6*6 none
process
CYP2D6*7 none
• couma
CYP2D6*8 none metabol
CYP2D6*9 decreased process
CYP2D6*10 decreased • lipid
metabol
CYP2D6*11 none
• isoquin
CYP2D6*12 none
alkaloid
CYP2D6*13 none metabol
CYP2D6*14 none process
CYP2D6*15 none • alkaloid

CYP2D6*17 decreased cataboli

process
CYP2D6*19 none
• oxidati
CYP2D6*20 none
CYP2D6*21 none demethy

CYP2D6*29 decreased • drug ca

process
CYP2D6*31 none
• heteroc
CYP2D6*38 none
metabol
CYP2D6*40 none process
CYP2D6*41 decreased • negativ
CYP2D6*42 none regulatio
binding
CYP2D6*68 none
• drug m
CYP2D6*92 none
process
CYP2D6*100 none •
CYP2D6*101 none monoter
CYP2D6 metabol
increased process
duplication
• xenobi
metabol
Ethnic factors in variability process
Race is a factor in the occurrence of • oxidati

CYP2D6 variability. The lack of the liver reductio

process
cytochrome CYP2D6 enzyme occurs
• arachid
approximately in 7–10% in white
acid met
populations, and is lower in most other
process
ethnic groups such as Asians and • negativ
African-Americans at 2% each.[14] The regulatio
occurrence of CYP2D6 ultrarapid cellular
metabolizers appears to be greater organofl

among Middle Eastern and North metabol

process
African populations.[15]
• long-ch
Caucasians with European descent fatty aci
biosynth
predominantly (around 71%) have the
process
functional group of CYP2D6 alleles,
• organic
while functional alleles represent only
metabol
around 50% of the allele frequency in
process
populations of Asian descent.[16] • exogen
drug cat
This variability is accounted for by the
process
differences in the prevalence of various
Sources:Amigo / Qu
CYP2D6 alleles among the Orthologs

populations–approximately 10% of Species Human Mou

whites are intermediate metabolizers, Entrez
due to decreased CYP2D6 function, 1565 n/a

because they appear to have the non-

Ensembl ENSG0000
functional CYP2D6*4 allele,[12] while
ENSG0000
approximately 50% of Asians possess
ENSG0000
the decreased functioning CYP2D6*10
ENSG0000
allele.[12]
ENSG0000
Ligands ENSG0000

Following is a table of selected UniProt

P10635 n/
substrates, inducers and inhibitors of
CYP2D6. Where classes of agents are
RefSeq
listed, there may be exceptions within (mRNA) NM_000
the class. NM_001025

Inhibitors of CYP2D6 can be classified RefSeq

NP_000
by their potency, such as: (protein)
NP_001020
Strong inhibitor being one that
causes at least a 5-fold increase in Location Chr n/a

the plasma AUC values of sensitive (UCSC) 22:

42.13
substrates metabolized through
–
CYP2D6, or more than 80% decrease
42.13
in clearance thereof.[17]
Mb
Moderate inhibitor being one that [2]
PubMed n/a
causes at least a 2-fold increase in search
the plasma AUC values of sensitive Wikidata

View/Edit Human

substrates metabolized through

CYP2D6, or 50-80% decrease in
clearance thereof.[17]
Weak inhibitor being one that causes at least a 1.25-fold
but less than 2-fold increase in the plasma AUC values of
sensitive substrates metabolized through CYP2D6, or 20-
50% decrease in clearance thereof.[17]
Selected inducers, inhibitors and substrates of CYP2D6
Substrates
Inhibitors Inducers
↑ = bioactivation by CYP2D6

All[18] tricyclic antidepressants, e.g. Strong Strong

imipramine[17]
Certain SSRIs glutethimide (hypnotic
amitriptyline[17]
fluoxetine[17][18] sedative)
etc.
paroxetine[17][18] Unspecified potency
Most[18] SSRIs (antidepressant), e.g.
bupropion[17][25] (non-SSRI dexamethasone[17]
fluoxetine[17]
antidepressant) (glucocorticoid)
[17]
paroxetine
quinidine[17][18] (class I antiarrhythmic rifampicin[17] (bactericidal)
fluvoxamine[17] agent)
haloperidol[40] (typical
[17][18]
venlafaxine (SNRI antidepressant) quinine[26] antipsychotic)
duloxetine[17] (SNRI, moderate sensitive substrates of cinacalcet[17] (calcimimetic)
CYP2D6[17])
ritonavir[18] (antiretroviral)
mianserin[18] (tetracyclic antidepressant)
cannabidiol[27]
mirtazapine[18] (antidepressant)
Moderate
opioids
codeine[17][18] ↑[into morphine][19] sertraline[17] (SSRI)

tramadol[17][18] ↑[into O-desmethyltramadol][19] duloxetine[17] (SNRI)

O-desmethyltramadol ↑[into N,O- terbinafine[17] (antifungal)

didesmethyltramadol] Weak

N-desmethyltramadol [inactive] ↑[into N,O- amiodarone[17] (antiarrhythmic)

didesmethyltramadol]
buprenorphine[28] (in opioid addiction)
oxycodone[17]
cimetidine[17] (H2-receptor antagonist)
hydrocodone ↑[into hydromorphone][20]
citalopram[17][29] (SSRI)
tapentadol
escitalopram[17][29][30] (SSRI)
antipsychotics, e.g.
methylphenidate [31]
haloperidol[17][18]
diltiazem [23]
risperidone[17][18]
felodipine [32][33][34]
perphenazine[17][18]
mirtazapine[35]
thioridazine[17][18]
Unspecified potency
zuclopenthixol[17][18]

iloperidone[17][18] antipsychotics
haloperidol[36][17]
aripiprazole[17][18]
perphenazine[17][36]
chlorpromazine[17][18]
thioridazine[36]
levomepromazine[18]
zuclopenthixol[36]
remoxipride[18]
chlorpromazine[17]
minaprine[17] (RIMA antidepressant)
hyperforin (St. Johns Wort)[37]
tamoxifen[17][18] ↑[into hydroxytamoxifen][21] (SERM)
antihistamines (H1-receptor antagonists)
beta-blockers
promethazine[38] (antipsychotic)
[17][18]
metoprolol
chlorphenamine[17]
 timolol[17][18] diphenhydramine[17]

alprenolol[17][18] hydroxyzine[17]

carvedilol[17] tripelennamine[17]

bufuralol[17] clemastine[17] (antihistamine and

anticholinergic)
nebivolol[17]
celecoxib[17] (NSAID)
propranolol[17]
clomipramine[17] (tricyclic
debrisoquine[17] (antihypertensive)
antidepressant)
Class I antiarrhythmics
cocaine[17] (stimulant)
flecainide[17][18]
doxorubicin[17] (chemotherapeutic)
propafenone[17][18]
metoclopramide[17] (antiemetic,
encainide[17][18]
prokinetic)
[17][18]
mexiletine
methadone[17] (analgesic and anti-
lidocaine [17] addictive)
sparteine[17] moclobemide[17] (antidepressant)
ondansetron[17][18] (antiemetic) niacin[39] (vitamin)
donepezil[17][18] (acetylcholinesterase inhibitor) nicotinamide[39] (vitamin)
phenformin[17][18] (antidiabetic) doxepin[17] (tricyclic antidepressant,
tropisetron[18] (5-HT3 receptor antagonist) anxiolytic)

stimulants halofantrine[17] (in malaria)

amphetamine[17] levomepromazine[17] (antipsychotic)
methoxyamphetamine[17] mibefradil[17] (calcium channel blocker)
dextromethamphetamine[17] midodrine[17] (α1 agonist)
NRI ticlopidine[17] (antiplatelet)
atomoxetine (Sensitive substrate of CYP2D6) [17]

chlorphenamine[17] (antihistamine)

dexfenfluramine[17] (serotoninergic anorectic)

dextromethorphan[17] ↑[into dextrorphan] (antitussive)

metoclopramide[17] (dopamine antagonist)

perhexiline[17] (antianginal agent)

phenacetin[17] (analgesic)

promethazine[17] (antihistamine antiemetic)

m-tyramine[22]

p-tyramine[22]

Calcium channel blocker

diltiazem (minor/moderate sensitive substrate) [23]

nifedipine (minor/moderate sensitive substrate)[24]

Dopamine biosynthesis …
 Biosynthetic pathways for catecholamines and trace
amines in the human brain[41][42][22]
AADC PNMT

L-Phenylalanine Phenethylamine N-Methylphenethylamine

AAAH
N-Methyltyramine
PNMT

AADC

L-Tyrosine p-Tyramine DBH

brain minor p-Octopamine

AAAH CYP2D6 pathway

PNMT
AADC
primary
pathway
L-DOPA Dopamine

Synephrine
DBH COMT

PNMT

Epinephrine Norepinephrine 3-Methoxytyramine

In humans, catecholamines and phenethylaminergic trace amines are

derived from the amino acid phenylalanine. It is well established that
dopamine is produced from L-tyrosine via L-dopa; however, recent evidence
has shown that CYP2D6 is expressed in the human brain and catalyzes the
biosynthesis of dopamine from L-tyrosine via p-tyramine.[22] Similarly,
CYP2D6 also metabolizes m-tyramine into dopamine.[22]

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Further reading
Smith G, Stubbins MJ, Harries LW, Wolf CR (December 1998).
"Molecular genetics of the human cytochrome P450
monooxygenase superfamily". Xenobiotica. 28 (12): 1129–65.
doi:10.1080/004982598238868 . PMID 9890157 .
Wolf CR, Smith G (1999). "Cytochrome P450 CYP2D6". IARC
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External links
Flockhart Lab Cyp2D6 Substrates Page at IUPUI
PharmGKB: Annotated PGx Gene Information for CYP2D6
 Human CYP2D6 genome location and CYP2D6 gene
details page in the UCSC Genome Browser.

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